Advances in technology in the last century have brought benefits to society but have resulted in a greater prevalence of stress in the daily lives of people at all levels of society. Our stress response mechanisms have not adapted at the same pace as advancing technology. The effect of stress on health and well being is well documented. See, for example, Robert M. Sapolsky, Why Zebra's Don't Get Ulcers-An Updated Guide to Stress, Stress Related Diseases and Coping, ISBN 0-7167-3210-6, Chapter 1, (5th Edition 2000), and George P. Chrousos and Philip W. Gold, “The Concepts of Stress and Stress System Disorders-Overview of Physical and Behavioral Homeostasis,” JAMA, Mar. 4, 1992, Vol. 267, No. 9. It is known that stress, particularly chronic stress, may cause or aggravate many conditions, including immunosuppression and susceptibility to infectious diseases, gastric conditions, sleep problems, depression, premature birth in expectant mothers, low birth weight, degeneration of brain neurons leading to memory and learning problems, elevated blood pressure, heart complications and stroke due to elevated blood lipid levels and other health complications.
Repeated exposure to acute stressors may lead to chronic stress. The acute stress response is commonly known as the “fight or flight” response. Acute stress is any stimulus or experience that is perceived as causing conflict or danger. In modern life, there exists a multitude of sources of acute stress, some examples of which include stress associated with interviews, public speaking, examinations, a dispute within a relationship, a traffic jam, being told some unpleasant news, or witnessing an unpleasant or disturbing scene. The “fight or flight” response promotes survival by protecting from bodily harm through providing the physical resources required either for conflict with the danger (fight) or to escape from the danger (flight). The response originates in the hypothalamus, which responds to a stressor by activating the sympathetic nerve endings in the adrenal medulla to produce epinephrine (adrenaline) as a part of the sympathetic-adrenal-medulla (SAM) system. Epinephrine (adrenaline) is secreted by the nerve endings in the adrenal medulla and norepinephrine (noradrenaline) is secreted by all other sympathetic nerve endings in the body that control relatively unconscious functions, including heart rate, digestion and salivary flow. It is epinephrine and norepinephrine that produce the “fight or flight” response in the organs of the body, preparing the mammal to respond to a stressor by increasing heart rate, increasing blood flow to muscles, diverting blood flow from the digestive system and inhibiting digestion, inhibiting saliva flow and dilating pupils, which are all desirable physiological responses in a survival threatening situation.
One method of measuring the response to an acute stressor in a mammal is to monitor the hypothalamus-pituitary-adrenal (HPA) system, and, in particular, the release of cortisol, corticotropin releasing hormone (CRH) and adrenocorticotrophic hormone (ACTH). Cortisol may be detected in saliva as a measure of response to a stressor. However, where cortisol is secreted in response to an acute stressor, it takes approximately twenty minutes after the onset of the stressor before the change in cortisol is detectable in saliva. Furthermore, additional time is required for the quantitative analysis of cortisol in saliva.
Given that the rapid onset of an acute stress response, or conversely the immediate physiological response to relaxation, occurs over a short time frame (generally on the order of seconds), measurement of changes of bodily functions controlled by the sympathetic nervous system would be useful in measuring stress or relaxation response. Accordingly, there remains a need for a time-independent measure of the acute stress or acute relaxation response of a mammal.
Another method of measuring the response to stress or relaxation is to quantify or observe physiological changes driven by the sympathetic nervous system. For example, some devices like mood rings and thumb press stress indicators, which rely on skin temperature changes, are simple however they only measure qualitative temperature differences. Other techniques, including lie detector type tests, such as those described in Japanese Kokai 11-034688, which rely on skin impedance changes, and thermal imaging techniques, such as those described in U.S. Pat. No. 5,771,261, which rely on skin temperature changes, may be used to supply quantitative information on the response to stress or relaxation, but these techniques are complicated and cumbersome.
Given the shortcomings of known methodology, there exists a need for a non-invasive, easy-to-use, time-independent and non-cumbersome method of measuring the state of the sympathetic nervous system as a means of measuring acute stress or relaxation response in a mammal.
The present invention addresses the problem of quantitatively measuring the immediate physiological response to acute stress or relaxation in a non-invasive, time-independent and easy-to-use method. We have surprisingly found that comparisons of the levels of oxyhemoglobin and deoxyhemoglobin in cutaneous blood supply provide a quantitative measure and a means of monitoring the acute stress or relaxation level of a mammal.